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At least 19 recordsLinked to original sources

PubMed1978

Isolation and characterization of defective interfering particle of Newcastle disease virus.

Newcastle disease virus grown in embryonated eggs was separated and purified by sucrose density gradient centrifugation into two distinct type of particles, B and T, the former being normal virus particles with high activities of hemagglutination, hemolysis, neuraminidase and infectivity, the latter being non-infectious virus particles with low activities of hemolysis and neuraminidase but high hemagglutination activity. B and T particles were shown to share a common antigen by immunodiffusion test. T particles were deficient in viral RNA, since they contained only 13s RNA in a small amount, whereas B particles possessed a large amount of 57s RNA and a small amount of 13s RNA. T particles interfered with the multiplication of normal Newcastle disease virus in primary cultures of chick embryo cells.

Animals↗

PubMed1976

The mediator of cellular immunity. XII. Inhibition of activated T cells by Newcastle disease virus.

Newcastle disease virus (NDV) can interact in at least two ways with rat T cells. By adsorbing to circulating lymphocytes, the virus can transiently deflect the cells from lymph nodes and inflammatory exudates induced in the peritoneal cavity. T cells are affected regardless of age, state of activation, or position in the mitotic cycle. The effect is reversible and is mediated not only by infectious (I)-NDV, but also by UV-NDV which cannot achieve a complete replication cycle in eggs. But I-NDV has another lasting effect on activated T cells. It is revealed in the failure of virus-treated thoracic duct lymphocytes to transfer cellular resistance to Listeria monocytogenes, delayed-type hypersensitivity to soluble antigens of the parasite, and the permanent exclusion of labeled S-phase lymphocytes from inflammatory foci. Activated T cells are inhibited by virus multiplicites which have little if any effect upon the proliferative potential of antigen-sensitive T cells or localization of labeled small lymphocytes in lymph nodes. The underlying mechanism has not been determined; however, there are reasons for thinking that NDV has a lethal effect upon activated T cells, because the latter are permissive for virus replication.

Animals↗

PubMed1978

Interaction between infectious bursal disease virus and Newcastle disease virus in chickens.

The Australian strain of infectious bursal disease virus (IBDV), 002/73, affected the response of chickens to Newcastle disease virus (NDV). The titre of serum antibodies to NDV in chickens infected with IBDV was significantly lower than that of birds infected with NDV alone. It also appeared that IBDV affected NDV excretion from chickens as NDV was more frequently isolated from chickens infected with IBDV, IBDV infection did not alter the pathogenicity of NDV in chickens. This Australian strain of IBDV therefore appeared to be immunodepressive in one-day-old chickens.

Animals↗

PubMed1977

Host cell modification of lymphocytic choriomeningitis virus and Newcastle disease virus altering viral inactivation by human complement.

Complement in human serum inactivated several enveloped viruses, but for some viruses the degree of inactivation depended on their passage history. In short, human serum detected cell-induced modifications of virions. Normal human serum, lacking detectable neutralizing antibodies to the virions, inactivated lymphocytic choriomeningitis virus (LCMV) and Newcastle disease virus (NDV) when the viruses were passed through some cell lines but not others. Host cell modification was further documented with LCMV since antibody to the cell (in conjunction with a complement source) inactivated virus produced by that cell. The mechanism by which human serum inactivated LCMV passed through L cells was determined. By using serum immunochemically depleted in the classical complement pathway component C4 and/or the alternative complement pathway component factor B, as well as other methods, it was shown that LCMV was inactivated via the classical complement pathway. Absorption and immune precipitation experiments indicated that the inactivation of LCMV by complement was mediated by natural antibody directed against the host (L-929) cell. NDV grown in chick embryo cells could be unactivated by either complement pathway in the absence of the other. A requirement for antibody could not be demonstrated in the NDV system. On the basis of these data it is proposed that alterations in virulence dependent upon passage of the virus in cells or animals may be partially explained by changes in virus sensitivity to human serum inactivation.

Animals↗

PubMedDate not supplied

Transmissibility of Australian strains of Newcastle disease virus.

The transmission of Newcastle disease virus strains from infected to direct-, indirect-, and aerosol-contact groups of chickens was studied. Chickens 7, 21, and 63 days old were used in separate trials. Chicken age and virus strain were found to be important in spread of the virus. Strain V4 spread quickly to all contact groups and was classed as highly transmissible, whereas strain JA failed to infect all contact chickens of each age group, thus spreading less efficiently than strain V4. The viruses spread more readily among the 2 older groups. The significance of the transmissibility of Newcastle disease virus vaccine is briefly discussed.

Age Factors↗

PubMed1978

The isolation of lentogenic strains of Newcastle disease virus in Australia.

Twelve isolations of Newcastle disease virus were made from 77 clinical samples from chickens from conjunctivitis, respiratory disease, proventriculitis and bursal atrophy. Nine of the isolations were made from chickens with conjunctivitis. The viruses were identified as Newcastle disease virus by inhibition of their haemagglutinins with specific antiserum to Newcastle disease virus. The viruses failed to kill chicken embryos after inoculation into the allantoic cavity and they were judged to be lentogenic strains. There was no evidence that the Newcastle disease viruses were responsible for any of the clinical conditions from which they were isolated. The presence of other agents in 10 of the samples was indicated by reduced production of haemagglutinin in allantoic fluids of infected embryos, by deaths of infected embryos, by the production of cytopathic changes in avian cell cultures and by electron microscopy. Three isolations of infectious bronchitis virus, 2 of avian adenovirus and one of avian reovirus were made. Other samples were suspected of containing infectious bronchitis virus and mycoplasmas, but these were not isolated. The Newcastle disease viruses failed to produce plaques in chicken embryo fibroblast cell cultures and they were separated from the contaminating agents by haemagglutination and elution followed by passage at terminal dilution in chick embryos. No Newcastle disease virus was isolated from 60 caecal tonsils and 60 lung samples from 9-week-old broiler chickens. Eight lung samples yielded mycoplasmas that caused haemadsorption in chicken cell cultures. The mycoplasmas were probably Mycoplasma gallisepticum.

Animals↗

PubMed1979

Depression of contact hypersensitivity to oxazolone in mice exposed to Newcastle disease virus.

The effect of Newcastle disease virus (NDV) on delayed hypersensitivity to oxazolone in CBA mice was studied. There was a significant impairment of the ability of mice to develop cutaneous hypersensitivity shortly after injection of the virus. The effect was evident when NDV was administered up to 2 days before or within 24 h after sensitization, suggesting that NDV interferes with the process of sensitization. The degree of depression was related to the dose of virus inoculated. NDV inactivated by UV irradiation or heat did not depress contact sensitivity to oxazolone. These data are considered to support the hypothesis that the depression is mediated by a direct interaction between lymphocytes and NDV.

Animals↗

PubMed1978

The isolation and characterisation of a Newcastle disease virus from an exotic parrot.

A newcastle disease virus was isolated from a salmon-crested cockatoo (Cacatua moluccensis) illegally introduced into Australia, Viral-characterisation and chicken-transmission studies indicated that the isolate, G5320/1, was a lentogenic pathotype. It caused a severe respiratory disease in chickens exposed oronasally at 1-day old and in chickens housed at 1 day of age with chickens infected with Newcastle disease virus. No harmful effects were detected in 5-week old chickens inoculated intravenously or oranasally with the virus.

Animals↗

PubMed1976

Acute encephalopathy caused by defective virus infection. I. Studies of Newcastle disease virus infections in newborn and adult mice.

An acute encephalopathy caused by a defective paramyxovirus infection was studied. Newcastle disease virus (ndv), given intracerebrally, caused neurologic disease and death in mice. Infected newborn mice died by the fourth day after inoculation, and abundant amounts of virus were recovered from their brains. Infected 4-week-old mice died by the eighth day, but only minimal amounts of virus, if any, were recovered. The brains of many moribund 4-week-old mice were histologically normal and contained no NDV antigen on fluorescent antibody staining. No serum antibody to NDV was detected. These features make this infection difficult to distinguish from a metabolic encephalopathy.

Age Factors↗

PubMed1978

Antigenic differences between strains of Newcastle disease virus.

Comparison of strains of Newcastle disease virus by kinetic neutralization tests and immunodiffusion tests (after virion disruption by ether and Tween 80) enabled antigenic differences to be demonstrated between four out of five strains tested. No correlation was demonstrated between the antigenic structure and virulence of these strains.

Antigens, Viral↗

PubMed1978

[Variability and the virulence of the Newcastle disease virus].

Six isolates of the Newcastle Disease virus (NDV), taken at different periods of time after provocation of immune birds with velogenous viscerotrophic strain, are used. It is shown that the virulence of the initial NDV challenge strain remains unchanges up the 46th day of persistence. The isolate, taken after 70 days of carriage, manifests a considerably decreased virulence. It is established that the reduced virulence is not genetically stable and reverts towards the initial one following passage through appropriate host organism. The latent infection with NDV is examined from ecological and practical aspects.

Animals↗

PubMed1977

Different pools of free myoinositol in chick-embryo cells as indicated by infection with Newcastle-disease virus.

Infection of chicken fibroblasts with Newcastle-disease virus indicates that cellular inositol is compartmented in at least two pools. Only the smaller pool is directly connected with the biosynthesis of phosphatidylinositol. Entrance of exogenous inositol into this pool is inhibited by phlorizin but not by the virus. Three hours after infection Newcastle-disease virus blocks the entrance of inositol from the small pool into one (or more) subsequent larger pool(s). About five hours after infection the virus enhances the catabolism of phosphatidylinositol in chicken cells and about seven hours after infection the permeability of the plasma membrane increases.

Animals↗

PubMedDate not supplied

[Synthesis of virus-specific RNA under conditions of homologous and heterologous interference by Newcastle disease virus].

Homologous and heterologous interference by Newcastle disease virus (NDV) was manifested in a marked inhibition of virus-specific RNA synthesis of both the interacting viruses. Inactivation of the interfering NDV by irradiation reduced its capacity to inhibit the synthesis of virus-specific RNA of the homologous virus, leaving its effect on the synthesis of RNA of the heterologous virus unchanged. In contrast, treatment of cell cultures with heparin leading to reduced interferon production eliminated the heterologous interference but did not affect the homologous interference.

Animals↗

PubMedDate not supplied

[Characteristics of 24S and 35S virus-specific RNA in cells infected with Newcastle disease virus].

The properties of 24S and 35S virus-specific RNAs of Newcastle disease virus were studied after denaturation. It was shown that 60-80% of 24S and 35SRNA consisted of agglomerates of molecules of virus-specific 18S RNA. Undissociable upon denaturation, 24S RNA contained mainly the same components as undenaturated RNA and consisted completely of sequences of virus-specifis 18S RNA. Undissociable 35S RNA contained no "heavy" heterogenous material present in the intact undenaturated RNA and 75% of it consisted os sequences of 18S virus-specific RNA. Some sequences present in undissociable 24S RNA were absent in undissociable 35S RNA. The aggregation of virus-specific na-transcripts and subsequent formation of covalent bonds between transcripts as well as possible formation of "solid" transcripts of the adjacent genes are discussed.

Newcastle disease virus↗

PubMed1977

Restitution of hemagglutinating activity to spikeless particles of HVJ (Sendai virus) by glycoprotein components of Newcastle disease virus.

Spikeless particles of HVJ (Sendai virus) lacking in hemagglutinating (HA) activity were obtained by enzymatic digestion of virions with trypsin followed by centrifugation through a sucrose gradient. When they were mixed with glycoprotein components of Newcastle disease virus (NDV) obtained by treatment of purified virions with deoxycholate (DOC), the mixture showed hemagglutination reaction, which was inhibited by anti-NDV serum, but not by anti-HVJ serum. Sedimentation profile of the HA active agents was then examined by centrifugation of the mixture of spikeless particles of HVJ (labeled with 3H-uridine) and glycoproteins of NDV (labeled with 14C-amino acid mixture). The results showed that the peak of HA activity had both of the radioactivities, and that the sedimentation rate of the HA was faster than that of spikeless HVJ but slower than that of intact HVJ. Electron micrographs of such HA active structures showed that they were morphologically closely similar to intact virion of HVJ, although they had neither hemolytic activity nor infectivity. The mixture of spikeless HVJ and glycoproteins of HVJ or NDV which were removed from virions by proteolytic enzymes, on the other hand, did not show any detectable hemagglutinating activity.

Deoxycholic Acid↗

PubMed1979

[Serological response and the viral carrier state in chickens infected with the pathogenic Newcastle disease virus].

Three groups of susceptible chickens were treated with Newcastle Disease vaccine, as follows: group I--orally, strain La Sota; group II--aerosole treatment, strain La Sota and group III--intramusculary, Komarov's vaccine. Varying HI antibody levels were observed following vaccine application. The average antibody titer of group I and II experimental chickens (40 in number for each group) was 25 days post vaccination respectively log2 = 3.47 and log2 = 6.2 while of group III (50 chickens) it was 14 days post vaccination log2 = 8.4. Aerosole challenge with velogenic viscerothropic strain of Newcastle Disease virus caused a sharp change in serum antibody titer. The low antibody titer in group I rose quickly post challenge while in groups II and III, on the contrary, it fell sharply. This characteristic dynamics is proposed for use as an indicator showing the presence of pathogenic virus in vaccinated birds. It was proven that pathogenic Newcastle Disease virus persisted in birds from group I for 40 days and 10% of them were in a state of latent infection (clinically healthy). The virus was isolated after method of organ cultures of tracheal explantates. It was established that the HI antibody level in the blood serum of virus carriers was higher as compared with that of the remaining birds in the group. The use of this fact as an indicator for beginning virusological investigations aiming to reveal latent Newcastle Disease infection is proposed.

Animals↗

PubMed1977

Isolation of type A influenza and Newcastle disease viruses from migratory waterfowl in the Mississippi flyway.

Twenty-seven chicken red blood cell agglutinating agents were isolated from 187 tracheal swabbings of apparently healthy migratory mallard ducks (Anas platyrhynchos) in the Mississippi flyway. Twenty-four of the isolants were type A influenza virus; 3 lentogenic Newcastle disease viruses were isolated. Isolations were not made from either 65 giant Canada geese (Branta canadensis) or 60 Franklins' gulls (Larus pipixcan).

Animals↗

PubMed1977

Host induced modifications of Newcastle disease virus virion polypeptides.

The polypeptide composition of Newcastle Disease Virus (NDV) virions grown in two host cell cystems--chorioallantlic membrane (CAM) and BHK-21 cells--was studied. Two strains of virus were compared, one highly virulent, the other completely avirulent. No significant differences in the polypeptide composition of the two strains of virus could be detected. However, differences were found in virions grown in different hosts, the same differences being found in both strains. An additional polypeptide is found in BHK grown virus which is not present in CAM grown virus and this is associated with a decreased relative amount of nucleocapsid protein in BHK grown virus. The possibility of this new polypeptide being a degradation product of the nucleocapsid protein is discussed. BHK grown virions also contain increased amounts of a polypeptide migrating to a position which might be expected of the FO precursor glycoprotein. However, in contrast to the FO polypeptide, this polypeptide does not appear to be glycosylated.

Animals↗